Early implantable pacemakers provided stimulus pulses at fixed rates, or within a range of rates that was externally programmable, to restore a normal resting heart rate to a patient suffering bradycardia. Such cardiac stimulation rates may meet the metabolic demand of the patient at rest or in low level exercise, but are generally inadequate to meet the demands of moderate to vigorous exercise. Sensor-controlled implantable cardiac pacemakers have been developed to attempt to adjust the rate of production of pacing pulses to meet metabolic demands, as dictated by the physiological condition of the patient in whom the pacemaker is implanted, utilizing parameters such as blood pH, body temperature, respiration rate, ventricular preejection period (PEP), or body motion or activity, for example. Many such sensor-controlled pacemakers are still inadequate to meet the demands of the patient due to limitations in sensitivity, specificity, and/or speed of response.
The type of rate adaptive pacemaker which relies on determining the activity, or body motion, of the patient to set the stimulus pulse rate has the advantage of the activity sensor being positioned within the case of the pacemaker, and not extending to a part of the patient's body removed from the pacemaker. Generally, an electromechanical sensor is included as part of such a pacemaker, and responds to being moved by producing an electrical signal which the pacemaker signal processing circuitry then interprets. Such an electromechanical sensor may be an accelerometer, positioned within the case of the pacemaker and cushioned from the case to detect acceleration of the body of the patient with the use of an inertial mass and appropriate detectors of movement of the mass. Alternatively, the activity, or motion, sensor may include a piezoelectric crystal attached to the interior of the pacemaker case to detect vibrations of the case, as indicative of movement of the patient's body. If it is determined that the patient's activity has increased, the pacemaker may respond by increasing its pacing pulse rate, in proportion to the sensor signal.
Activity/motion sensors are incorporated into a majority of rate adaptive pacemakers available today because they provide sufficient rate compensation for most conditions, offer fast response time, and are easy to program. However, such sensor-controlled pacemakers may lack specificity, since not all movement detected by an electromechanical sensor is activity by the patient that demands an increased rate of heartbeat. For example, the activity sensor may be detecting motion due to the patient riding in an automobile, or in an elevator. Such circumstances would normally not require an increased heart rate. The activity/motion-controlled pacemaker may not be able to distinguish such movement of the patient from movement associated with the patient exercising, and needing an increased heart rate. As a result, the pacemaker is conditioned to provide an increasing pacing rate at times when the patient may not require such a rate, and which may be harmful under certain clinical conditions. Another example in which the activity sensor response is not in proportion to the patient's activity occurs when the patient is going down stairs. In such a case, an activity sensor-controlled pacemaker generally provides a much greater pacing rate than is actually needed by the patient, since body motion and vibration are more intense going down stairs than, for example, going up stairs, although the latter exercise is the more stressful for the patient.
All rate responsive pacemakers have the capability of being externally programmed for a minimum and a maximum pacing rate, which are generally adjusted according to the patient's age, clinical condition, and the expected level of physical activity. The minimum pacing rate is called Lower Rate and the maximum pacing rate is called Upper Rate. Setting the maximum pacing rate at a relatively low level may offer some protection against excessive pacing rates caused by lack of specificity of the activity sensor, but will deprive the patient of the needed rate under heavy exercise conditions. Other sensors which detect physiological cardiac signals, such as PEP, are more specific to increased metabolic demands, but are less sensitive, sometimes not responding adequately under low level exercise or postural changes.
With rate adaptive pacemakers using non-physiological sensors, such as activity/motion sensors, the possibility exists that the heart will be paced inappropriately fast for the prevailing metabolic demands. It would thus be advantageous and desirable to equip a rate-responsive cardiac pacemaker with a mechanism for setting an automatically variable upper rate limit (URL) for the stimulus signal provided by the pacemaker in response to the signal generated by the activity sensor, wherein the URL is determined by the level of change of a physiological parameter. A large activity-controlled pacing rate increase would thus be allowed only if there is confirmation of a significant increase in metabolic demand, thus increasing the specificity of the rate-adaptive pacemaker, and adding an important safety feature. The present invention provides such method and apparatus.
During cardiac systole, blood pressure in the aorta and pulmonary artery rises until the aortic and pulmonic heart valves close, after which arterial pressure declines during diastole. PEP is the time interval between the beginning of the cardiac cycle, initiated by the QRS complex of the electrocardiogram, or by a pacing pulse, whichever is first to occur and the commencement of ventricular ejection. The QRS complex pulse, or a pacing pulse, causes electrical depolarization of the heart, including, ultimately, depolarization of the ventricles, and ventricular contraction. There is an initial period of ventricular contraction during which muscular contraction occurs but no change occurs in the volume of the ventricles, there is no ejection of blood from the ventricles, and pressure in the ventricles rises. This phase is called isovolumic contraction time (IVCT), and constitutes most of the duration of PEP. During IVCT, pressure within the ventricles rises until the ventricle pressure exceeds the back pressure in the aorta and the pulmonary artery to open their respective heart valves. PEP ends as soon as the aortic and pulmonic valves open and blood flows into the aorta and pulmonary arteries, causing ventricular volume to gradually decrease as blood is emptied into these blood vessels. PEP is thus the time interval between the beginning of the cardiac cycle, marked by the QRS waveform, or by a pacing pulse, whichever is first to occur, and the commencement of ventricular ejection. For a given patient, the IVCT varies with metabolic demands, and, therefore, the PEP varies accordingly.
The duration of the PEP is primarily determined by the speed of contraction of muscle fibers of the myocardium, that is, the myofibrils. The faster the myofibrils contract, the faster the level of back pressure in the aorta and pulmonary arteries will be reached in the ventricle, and the shorter the PEP will be. Therefore, PEP is an indicator of the contraction ability of the heart, or contractility. That is, as contractility increases, PEP shortens. During exercise, or when the body is subject to stress, whether it is mental or physical, there is an increase in tone of the sympathetic nervous system and an increase in release of catecholamines into the blood stream, both of which enhance the metabolic activity of the heart musculature to increase contractility and, concurrently, heart rate, to effect the necessary response to the increased activity or stress. Under stress conditions, it would be expected that heart rate would increase in proportion to PEP shortening, both being guided by the same neuro-hormonal stimulation. During artificial increasing of pacing at rest, however, there is no shortening of PEP. Furthermore, under such conditions, PEP may even tend to lengthen due to reflex hemostatic or hemodynamic factors. Any increase in heart rate not associated with a corresponding shortening of PEP may thus be considered either inadequate or excessive, compared to the needs of the patient under the prevailing conditions.
Although the onset of PEP is unique, being signaled by the onset of electrical depolarization of the ventricles, the end of PEP may be determined in several ways. One technique uses the onset of rise in pulmonary artery or aortic pressure as a signal of the end of ejection. Another method uses Doppler flow indicators to signal the onset of blood passage through the arteries. A third technique measures intraventricular impedance as an indicator of ventricular volume. Intraventricular impedance is known to reciprocally reflect intraventricular blood volume, thus the onset of ventricular impedance increase will also signal the onset of ventricular ejection, that is, the end point of PEP.
Various techniques are known for monitoring intracardiac impedance, generally utilizing two or more electrodes positioned within a heart chamber. For example, my U.S. Pat. No. 4,865,036 discloses measuring intraventricular impedance using three electrodes positioned within the ventricle and an applied high frequency signal, with voltage changes across two of the electrodes detected to monitor the movement of blood into and out of the ventricle. My U.S. Pat. No. 5,154,171 discloses techniques for sensing intracardiac impedance by monitoring the amplitude modulation of the high frequency signal applied across electrodes by changes in the ventricular volume, utilizing two or more electrodes. My U.S. Pat. No. 5,179,949 also discusses impedance measurement whereby a driving signal is delivered to intraventricular electrodes and the resulting voltage is detected from the same electrodes to monitor changes in the blood volume through resulting impedance changes. U.S. Pat. No. 4,686,987 also utilizing two intraventricular electrodes across which an oscillatory signal is applied, and the amplitude modulation of the signal across the same two electrodes, due to changes of the volume of blood in the heart chamber effecting impedance between the electrodes, is analyzed. U.S. Pat. No. 4,773,401 discloses interpreting the intraventricular waveform to determine the end of PEP. U.S. Pat. No. 5,562,711 also discusses using two or more electrodes in sensing intraventricular impedance.